PMID- 18435423
OWN - NLM
STAT- MEDLINE
DCOM- 20080811
LR  - 20131121
IS  - 0887-4476 (Print)
IS  - 0887-4476 (Linking)
VI  - 62
IP  - 7
DP  - 2008 Jul
TI  - In vivo and in vitro ethanol exposure in prenatal rat brain: GABA(B) receptor 
      modulation on dopamine D(1) receptor and protein kinase A.
PG  - 534-43
LID - 10.1002/syn.20522 [doi]
AB  - We have investigated the effects of prenatal ethanol exposure on GABA(B) 
      receptors (GABA(B)Rs), protein kinase A (PKA), and DA D(1) receptor (DAD(1)R) 
      expressions. GABA(B1)R and GABA(B2)R showed different age-dependent expressions 
      in in vivo fetal rat forebrain from gestational days (GD) 15.5 to 21.5 upon 10% 
      ethanol treatment to mother, with and without baclofen at a dose of 10 mg/kg body 
      weight/day. The protein level changes could not be attributed to changes in the 
      level of transcription since GABA(B)R mRNA presented different expression 
      patterns upon in vivo ethanol treatment. Using in vitro cultivated cortical 
      neurons from GD 17.5 fetuses, we also explored the modulatory effects of ethanol 
      on PKA and DAD(1)R through GABA(B)Rs, under 50 microM baclofen and 100 microM 
      phaclofen administrations, with or without 100 mM of ethanol treatment in the 
      culture media. The results showed that 20 min ethanol treatment without baclofen 
      or phaclofen had increasing effects on both the GABA(B)Rs. Further, baclofen and 
      phaclofen administration significantly affected PKA and GABA(B)R levels upon 20 
      min and 1 h ethanol treatment. In contrast, DAD(1)R showed increasing effects 
      upon ethanol treatment, which was modulated by GABA(B)R's agonist baclofen and 
      antagonist phaclofen. Therefore the present study suggested that the GABA(B)R 
      activity could modulate ethanol's cellular effects, which possibly including PKA 
      and DAD(1)R activities, and may be an underlying cause of ethanol's effects.
FAU - Lee, H Y
AU  - Lee HY
AD  - Division of Life Science, College of Natural Sciences and Applied Life Science 
      (Brain Korea 21), Gyeongsang National University, Chinju 660-701, South Korea.
FAU - Naha, N
AU  - Naha N
FAU - Li, S P
AU  - Li SP
FAU - Jo, M J
AU  - Jo MJ
FAU - Naseer, M I
AU  - Naseer MI
FAU - Park, M S
AU  - Park MS
FAU - Park, T J
AU  - Park TJ
FAU - Chung, B C
AU  - Chung BC
FAU - Kim, M O
AU  - Kim MO
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Synapse
JT  - Synapse (New York, N.Y.)
JID - 8806914
RN  - 0 (Central Nervous System Depressants)
RN  - 0 (GABA Agonists)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (Receptors, GABA-B)
RN  - 3K9958V90M (Ethanol)
RN  - EC 2.7.11.11 (Cyclic AMP-Dependent Protein Kinases)
RN  - H789N3FKE8 (Baclofen)
SB  - IM
EIN - Synapse. 2010 Jul;64(7):578. Naseer, M L [corrected to Naseer, M I]
MH  - Alcohol-Induced Disorders, Nervous System/*metabolism/physiopathology
MH  - Animals
MH  - Baclofen/pharmacology
MH  - Brain/*drug effects/embryology/physiopathology
MH  - Cells, Cultured
MH  - Central Nervous System Depressants/pharmacology
MH  - Cyclic AMP-Dependent Protein Kinases/*drug effects/metabolism
MH  - Drug Administration Schedule
MH  - Drug Interactions/physiology
MH  - Ethanol/pharmacology
MH  - Female
MH  - GABA Agonists/pharmacology
MH  - Gene Expression Regulation/drug effects
MH  - Male
MH  - Pregnancy
MH  - Prenatal Exposure Delayed Effects/*metabolism/physiopathology
MH  - RNA, Messenger/drug effects/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Dopamine D1/*drug effects/genetics/metabolism
MH  - Receptors, GABA-B/*drug effects/genetics/metabolism
MH  - Up-Regulation/drug effects/physiology
EDAT- 2008/04/26 09:00
MHDA- 2008/08/12 09:00
CRDT- 2008/04/26 09:00
PHST- 2008/04/26 09:00 [pubmed]
PHST- 2008/08/12 09:00 [medline]
PHST- 2008/04/26 09:00 [entrez]
AID - 10.1002/syn.20522 [doi]
PST - ppublish
SO  - Synapse. 2008 Jul;62(7):534-43. doi: 10.1002/syn.20522.